阿托伐他汀对冠状动脉微栓塞后非梗死区心肌炎症的影响

目的：探讨阿托伐他汀干预治疗对冠状动脉微栓塞（CME）后非梗死区心肌炎症的影响。方法：给清洁级雄性新西兰兔选择性经左前降支（LAD）注入微栓子颗粒悬液建立CME模型,将36只新西兰兔随机分为CME组（模型组）、阿托伐他汀（atrovastatin）干预组及对照组,每组12只（n=12）。于术后7d处死,取左心室乳头段心肌经HE染色后,观察梗死心肌并检测梗死面积。用ELISA法及RT-PCR检测肿瘤坏死因子α（TNF-α）、白介素6（IL一6）及其基因在非梗死区（右室）心肌中的表达。结果：前降支动脉微栓塞后,非梗死区右室心肌中白细胞浸润明显增多,TNF-α、IL-6蛋白及其基因的表达显著增强。与未处理组相比,阿托伐他汀可显著抑制CME后右室心肌中白细胞浸润及TNF-α、IL-6蛋白及其基因的表达（均P〈0．01）。结论：冠脉微栓塞后,炎症反应的激活不仅局限于梗死灶,且累及非梗死区心肌。阿托伐他汀可显著抑制CME后非梗死区心肌炎症反应。     

阿托伐他汀对冠状动脉微栓塞后非梗死区心肌炎症的影响

目的:探讨阿托伐他汀干预治疗对冠状动脉微栓塞（CME）后非梗死区心肌炎症的影响。方法: 给清洁级雄性新西兰兔选择性经左前降支(LAD)注入微栓子颗粒悬液建立CME模型，将36只新西兰兔随机分为CME组（模型组）、阿托伐他汀（atrovastatin）干预组及对照组，每组12只(n=12)。于术后7 d处死，取左心室乳头段心肌经HE染色后，观察梗死心肌并检测梗死面积。用ELISA法及RT-PCR检测肿瘤坏死因子α（TNF-α）、白介素6（IL-6）及其基因在非梗死区（右室）心肌中的表达。结果: 前降支动脉微栓塞后，非梗死区右室心肌中白细胞浸润明显增多，TNF-α、IL-6蛋白及其基因的表达显著增强。与未处理组相比，阿托伐他汀可显著抑制CME后右室心肌中白细胞浸润及TNF-α、IL-6蛋白及其基因的表达(均P<0.01)。结论: 冠脉微栓塞后，炎症反应的激活不仅局限于梗死灶，且累及非梗死区心肌。阿托伐他汀可显著抑制CME后非梗死区心肌炎症反应。     

阿托伐他汀对2型糖尿病大鼠心肌炎症的影响

目的:探讨核转录因子-кB(NF-кB)、肿瘤坏死因子(TNF-α)及基质金属蛋白酶-9(MMP-9)在2型糖尿病大鼠心肌中的表达及阿托伐他汀对其影响.方法:将60只SD大鼠随机分为对照组(N组),糖尿病组(D组)和阿托伐他汀处理组(A组).采用放射免疫法检测血浆及心肌TNF-α.采用RT-PCR方法检测各组大鼠心肌组织中NF-кB、TNF-α及MMP-9的mRNA表达水平,用免疫组织化学染色法检测其蛋白表达.结果:D组大鼠血和心肌中TNF-α浓度较N组明显升高(P＜0.01),大鼠心肌组织中NF-кB及TNF-α、MMP-9 mRNA及蛋白表达较N组明显增加(P＜0.01).A组用阿托伐他汀处理12周后,NF-кB及TNF-α、MMP-9 mRNA及蛋白表达较D组明显降低(P＜0.05或P＜0.01).结论:阿托伐他汀可抑制糖尿病大鼠心肌组织中NF-кB及TNF-α、MMP-9的表达,对大鼠2型糖尿病性心肌病的炎症有一定防治作用.     

阿托伐他汀短期治疗慢性心力衰竭的临床观察

目的观察短期应用阿托伐他汀对慢性心力衰竭（CHF）患者心功能、血清肿瘤坏死因子-α（TNF-α）和白介素-6（IL-6）水平的影响。方法选择50例CHF患者随机分成治疗组27例和对照组23例。所有CHF患者均给予常规治疗，治疗组在此基础上加用阿托伐他汀10mg／次，1坎／d，晚餐后顿服，治疗4周。治疗前、后分别测量左室射血分数（LVEF）、TNF-α、IL-6和血脂水平。结果两组患者治疗前、后LVEF、TNF-α、IL-6间差异均有显著性意义（P〈0．01）；两组患者治疗前后差异亦均有显著性意义（P〈0．05）；治疗组患者治疗前、后TC、TG、LDL—C间差异均有显著性意义（P〈0．01）；两组患者治疗后TC、LDL—C间差异亦均有显著性意义（P〈0．05）。结论短期应用阿托伐他汀可以降低CHF患者的TNF-α和IL-6水平，改善心功能，其作用机制考虑可能与他汀类药物的非调脂作用有关。     

阿托伐他汀对大鼠冠状动脉微栓塞后血小板-白细胞聚集体的影响

目的探讨大鼠冠状动脉微栓塞(CME)后外周血血小板-白细胞聚集体(PLA)和CD62P的变化及阿托伐他汀对其的影响。方法通过左心室内注射自体微血栓,同时短暂夹闭主动脉建立CME模型。36只SD大鼠随机分为未治疗组及阿托伐他汀干预组、假手术组,每组12只,于术后7 d处死。采用流式细胞术检测CME大鼠及治疗组大鼠PLA和CD62P。结果 CME大鼠PLA、CD62P均显著高于阿托伐他汀干预组和假手术组,阿托伐他汀显著抑制CME后PLA和CD62P表达(P<0.05或P<0.01)。结论 PLA、CD62P的测定反映CME后血栓形成及炎症激活,阿托伐他汀显著抑制血小板活化及炎症反应。     

罗格列酮联合阿托伐他汀对单核细胞分泌肿瘤坏死因子α的影响

目的 研究罗格列酮联合阿托伐他汀干预对无糖尿病的急性冠脉综合征（ACS）患者外周血单核细胞分泌肿瘤坏死因子α（TNF-α）的影响。方法 分离无糖尿病的ACS患者外周血单核细胞,设置对照组（等容积的二甲基亚砜）、阿托伐他汀（1 μmol/L）组、罗格列酮（1 μmol/L）组及二者联合组（阿托伐他汀1 μmol/L加罗格列酮1 μmol/L组） 4个组,分别与所分离的外周血单核细胞共同孵育24 h后,用夹心酶联免疫吸附测定法检测细胞培养上清液TNF-α,用逆转录聚合酶链反应（RT-PCR）测定TNF-α mRNA的表达。结果 与对照组相比较,阿托伐他汀组、罗格列酮组及联合组对无糖尿病ACS患者外周血单核细胞分泌TNF-α［分别为(229±24)ng/L、(236±28)ng/L、(159±29)ng/L vs (306±40)ng/L,均P<0.05］及TNF-α mRNA的相对半定量吸光值（A）比值（分别为0.35±0.12,0.39±0.11,0.26±0.06 vs 0.78±0.14,均P<0.05）均降低,且罗格列酮联合阿托伐他汀组比阿托伐他汀组、罗格列酮组降低更显著（均P<0.05）。结论 阿托伐他汀和罗格列酮都可通过降低无糖尿病的ACS患者外周血单核细胞产生分泌TNF-α,发挥阿托伐他汀和罗格列酮的抗炎作用,且二者联合干预具有协同作用,防治效果更佳。     

核因子-κB激活在大鼠冠状动脉微栓塞后的心肌组织中的作用及机制

目的 探讨核因子-κB(NF-κB)激活在冠状动脉微栓塞(CME)后心肌组织中的作用及机制.方法 清洁级雄性SD大鼠88只,其中64只经左心窜内注射自体微血栓、同时短暂夹闭主动脉建立大鼠CME模型后,随机分为未治疗组及二硫代氨基甲酸吡咯烷(PDTC)干预组,分别于术后1、3、7、14 d处死;余24只为假手术组.电泳迁移率改变分析(EMSA)检测不同时间点心肌组织NF-κB DNA结合活性,Western blot测定肿瘤坏死因子α(TNFα)、白细胞介素-6(IL-6)及细胞间黏附分子-1(ICAM-1)的表达水平,实时聚合酶链式反应检测TNFα、IL-6及ICAM-1 mRNA 表达含量.结果 NF-κB DNA结合活性在CME后1 d增高,3 d时达到高峰;7 d时明显降低,14 d时与假手术组无显著性差异.CME组在不同观察时间点心肌TNFα、IL-6、ICAM-1蛋白及基因的表达较假手术组均明显增强(P＜0.05).NF-κB DNA结合活性与TNFα、IL-6、ICAM-13种细胞因子的mRNA表达水平均呈显著正相关(分别是r=0.72,P＜0.05;r=0.94,P＜0.01;r=0.62,P＜0.05).NF-κB特异性抑制剂PDTC干预显著抑制CME后心肌中TNFα、IL-6及ICAM-1蛋白及mRNA的表达(P均＜0.05),同时也改善心功能.结论 CME后NF-κB激活促使炎性因子TNFα、IL-6、ICAM-1在基因及蛋白水平明显上调,是诱导CME心肌炎症反应、心功能减低的重要早期事件.     

大剂量氟伐他汀短期治疗对老年不稳定性心绞痛患者血清可溶性细胞黏附分子和肿瘤坏死因子-α水平的影响

目的探讨大剂量氟伐他汀短期治疗对老年不稳定性心绞痛患者血清中可溶性细胞间黏附分子-1（sICAM-1）、可溶性血管细胞黏附分子-1（sVCAM-1）和肿瘤坏死因子-α（TNF-α）水平的影响。方法将56例老年不稳定性心绞痛患者随机分为常规治疗组和大剂量治疗组,两组患者均给予抗心绞痛常规治疗,常规治疗组给予氟伐他汀40mg／d,大剂量治疗组给予氟伐他汀80mg／d,入院当日和治疗1个月时检测患者血清中sICAM-1、sVCAM-1和TNF-α水平。结果两组患者治疗后血清sICAM-1、sVCAM-1和TNF-α水平均较治疗前明显降低（P〈0．05）,但组间比较差异无统计学意义（P〉0．05）。结论大剂量氟伐他汀短期治疗不能进一步降低老年不稳定性心绞痛患者血清sICAM-1、sVCAM-1和TNF-α水平。     

老年ACS患者血浆sICAM-1和sE-selectin的表达及阿托伐他汀对其影响

目的探讨老年急性冠脉综合征（ACS）患者血浆可溶性细胞间黏附分子-1（sICAM-1）和可溶性E-选择素（sE-selectin）的表达及阿托伐他汀对其影响。方法用ELISA法测定90例ACS患者和40例稳定性心绞痛（SAP）患者血浆sICAM-1和sE-selectin水平。同时将ACS患者随机分为高脂血症常规治疗组（A组）、高脂血症阿托伐他汀治疗组（B组）、非高脂血症常规治疗组（C组）、非高脂血症阿托伐他汀治疗组（D组）;B、D组在常规治疗的基础上每日口服10 mg阿托伐他汀,共8周。检测各组治疗前后血浆sICAM-1和sE-selectin水平变化。结果ACS组sICAM-1和sE-selectin水平均高于SAP组（P〈0.05,〈0.01）;阿托伐他汀治疗后,B、D组sICAM-1和sE-se-lectin水平较治疗前降低。结论血浆sICAM-1和sE-selectin水平与不同类型冠心病斑块稳定性有关,阿托伐他汀具有抑制细胞黏附分子表达,稳定动脉粥样硬化斑块的作用。     

实验性肺血栓栓塞症大鼠肺炎症反应的变化及阿托伐他汀的干预作用

目的探讨实验性肺血栓栓塞症大鼠肺炎症反应的变化及阿托伐他汀的干预作用。方法 42只大鼠随机分为假手术组(Sham组)、肺栓塞模型组(PTE组)、阿托伐他汀干预组(Statin组)。采用自体血栓回输法建立肺栓塞大鼠动物模型,取动脉血行血气分析,取肺组织行常规病理检查,免疫组化测定P38促分裂原活化蛋白激酶(P38MAPK)及TNF-α在肺组织中的表达。结果 PTE组明显缺氧,且肺组织炎症损伤较Statin组明显。PTE组肺组织P38MAPK、TNF-α表达较Sham组表达增强,Statin组与PTE组相比表达减弱,差异均有统计学意义(P均<0.05)。结论急性肺动脉栓塞可引起P38MAPK信号通路参与的炎症反应的激活,阿托伐他汀可以从某种程度上抑制P38MAPK、TNF-α的表达,从而减轻炎症反应。     

氧化苦参碱对急性胰腺炎患者外周血TNF-α，IL-1和IL-6水平影响及临床疗效观察

[目的]观察氧化苦参碱对急性胰腺炎（acute pancreastitis,AP）患者血清肿瘤坏死因子-α（TNF-α）,白细胞介素-1（IL-1）和白细胞介素-6（IL-6）水平及临床疗效的影响。[方法]60例AP患者随机分为2组,对照组30例,给予止血、补液等常规处理;治疗组30例,在常规处理基础上加用氧化苦参碱治疗。观察2组治疗前、治疗第4天和治疗第7天血清TNF-α、IL-1和IL-6水平的变化。同时评价2组间白细胞恢复正常时间、血淀粉酶恢复时间、腹痛缓解时间。[结果]治疗第4天时2组TNF-α、IL1和IL-6水平无明显差异（P〉0．05）,治疗第7天时,以上3项指标治疗组较对照组下降（P〈0．05）。治疗组白细胞恢复正常时间、血淀粉酶恢复正常时间、腹痛缓解时间较对照组缩短1．13～2．58d。[结论]氧化苦参碱能早期抑制AP患者炎症细胞因子TNF-α、II,1和II,6的水平,从而控制炎症的发展,尽早减轻AP的临床症状,改善患者的预后,值得在有条件的医院进一步推广应用。     

粒细胞集落刺激因子影响冠状动脉微栓塞后心肌细胞凋亡的研究

目的 探讨粒细胞集落刺激因子对大鼠冠状动脉(冠脉)微栓塞后心肌细胞凋亡及左心室功能的影响. 方法 68只雄性SD大鼠,随机分成微栓塞组24只、粒细胞集落刺激因子组24只和假手术组20只.微栓塞组和粒细胞集落刺激因子组升主动脉夹闭后自左心室腔内注入自体微血栓,造成冠脉微栓塞,假手术组注入等量生理盐水.粒细胞集落刺激因子组术后2 h起给予皮下注射重组人粒细胞集落刺激因子100 μg·kg-1·d-1,持续5 d,其余两组给予生理盐水.术后3 d、1周、2周及4周处死大鼠.各组心肌样品中以实时定量聚合酶链式反应法(real time PCR)检测Bcl-2、Bax、Fas及FasL的mRNA表达,并计算Bcl-2/Bax比值,以Western blot蛋白印迹法检测Caspase-3活性及裂解多聚二磷酸腺苷-核糖聚合酶(PARP)蛋白表达水平,脱氧核糖核苷酸末端转移酶介导的缺口末端标记法检测凋亡细胞及有创压力传感器记录左心室血流动力学改变. 结果 与假手术组比较,微栓塞组术后Bel-2、Bax、Fas及FasL的mRNA表达均有不同程度升高,Bcl-2/Bax比值降低(0.28±0.04和2.98±0.49),Caspase-3及裂解PARP蛋白表达增强(0.762±0.129和0.133±0.027;0.992±0.146和0.386±0.074),心肌细胞凋亡指数升高(17.2±1.9和1.2±0.6),左心室收缩压(LVSP)及左心室内压最大上升和下降速率(±dp/dtmax)明显降低(P<0.05或P<0.01);与微栓塞组比较,粒细胞集落刺激因子组术后Bcl-2的mRNA表达增强、Bax、Fas及FasL的mRNA表达均有不同程度降低,Bcl-2/Bax比值升高(2.07±0.29和0.28±0.04),aspase-3及裂解PARP蛋白表达减弱(0.371±0.041和0.762±0.129;0.548±0.093和0.992±0.146),心肌细胞凋亡指数降低(6.1±1.0和17.2±1.9),LVSP及±dp/dtmax明显升高(P<0.05或P<0.01). 结论 徽栓塞可导致心肌细胞凋亡,降低左心室功能;粒细胞集落刺激因子通过减轻微栓塞后心肌细胞凋亡,改善左心室功能.     

冠状动脉微栓塞后MCP-1变化的实验研究

目的经导管建立急性冠状动脉微栓塞模型，检测微栓塞后单核细胞趋化因子-1（monocyte chemotactic protein．1，MCP-1）的变化情况。方法12只小型猪，通过导管方法建立急性冠脉微栓塞模型，观察急性期（微栓塞前、微栓塞后2h、6h）及慢性期（微栓塞前、微栓塞后1周）血清中MCP-1浓度变化，RT-PCR观察心肌组织中MCP-1及粒细胞变化。结果MCP-1随时间变化逐渐增加，MCP-1存2h有明显增加，与基础相比P〈0．05；6 h MCP-1与基础相比P〈0．01。1周时，而MCP-1与微栓塞前相比没有明艟变化（P〉0．05），心肌组织RT．PCR显示MCP-1 mRNA表达只在6h明显升高（P〈0．05），1周时不再升高（P〉0．05）。微栓塞1周后前壁心肌组织病理切片计数测得粒细胞为（103．0±49．4），后壁测得为（43．9±24．0），两者相比有显著差异性（P〈0．05）。结论冠脉微栓塞后m【清MCP一1呈现先升高后下降趋势，心肌组织MCP-1 mRNA只在微栓塞后6h升高。     

Homocysteine and markers of inflammation in acute coronary syndrome

BACKGROUND:

An elevated level of homocysteine (Hcy) has been shown to be a cardiovascular risk factor in the majority of research studies. Recently, it was found to be associated with new risk factors such as inflammatory markers.

OBJECTIVES:

To investigate the distribution of plasma total Hcy (tHcy) and the levels of inflammatory markers in patients with acute coronary syndrome (ACS), and to evaluate the association between these parameters and the severity of the disease.

METHODS:

A total of 122 patients with ACS and 80 control subjects were recruited from the cardiac intensive care unit of the Military Hospital of Tunis, Tunisia. Lipid profile and the levels of tHcy, high-sensitivity C-reactive protein (HsCRP), interleukin (IL)-6, IL-8, IL-1β and tumour necrosis factor-alpha (TNFα) were determined for all participants. The distribution of these parameters were compared between groups and according to the number of diseased vessels in patients with ACS.

RESULTS:

ACS patients had significantly elevated levels of tHcy (P<0.01), HsCRP (P<0.001), IL-6 (P<0.001), TNFα (P<0.001), folates (P<0.05) and vitamin B₁₂ (P<0.001), but lower high-density lipoprotein cholesterol (P<0.05) levels. The analysis of the association between these parameters and the number of diseased vessels showed significant differences in tHcy, HsCRP, IL-6 and TNFα, with positive correlations. Significantly negative correlations were found between the number of diseased vessels and folate (r=−0.34; P<0.01), and vitamin B₁₂ (r=−0.22; P<0.01).

CONCLUSION:

Elevated levels of tHcy, IL-6, TNFα and HsCRP appear to be associated with a greater number of diseased arteries and, consequently, the severity of coronary artery disease.     

Oxidative modification of tropomyosin and myocardial dysfunction following coronary microembolization.

AIMS: We addressed a potential mechanism of myocardial dysfunction following coronary microembolization at the level of myofibrillar proteins. METHODS AND RESULTS: Anaesthetized pigs underwent intracoronary infusion of microspheres. After 6 h, the microembolized areas (MEA) had decreased systolic wall thickening to 38 +/- 7% of baseline and a 2.62 +/- 0.40-fold increase in the formation of disulphide cross-bridges (DCB) in tropomyosin relative to that in remote areas. The impairment in contractile function correlated inversely with DCB formation (r = -0.68; P = 0.015) and was associated with increased TNF-alpha content. DCB formation was reflected by increased tropomyosin immunoreactivity and abolished in vitro by dithiothreitol. Ascorbic acid prevented contractile dysfunction as well as increased DCB and TNF-alpha. In anaesthetized dogs, 8 h after intracoronary microspheres infusion, contractile function was reduced to 8+/-10% of baseline and DCB in MEA was 1.48+/-0.12 higher than that in remote areas. In conscious dogs, 6 days after intracoronary microspheres infusion, myocardial function had returned to baseline and DCB was no longer different between remote and MEA. Again contractile function correlated inversely with DCB formation (r = -0.83; P = 0.005). CONCLUSION: Myofibrillar protein oxidation may represent a mechanistic link between inflammation and contractile dysfunction following coronary microembolization.     

Effects of simvastatin and atorvastatin on inflammation markers in plasma

OBJECTIVES: To study the effect of statins on plasma markers for inflammation. DESIGN: Patients with hypercholesterolemia were randomized in one of the following treatments: Simvastatin (S) + placebo: S 40 mg for 6 weeks - S 80 mg for 6 weeks - S 80 mg for 24 weeks and Atorvastatin (A) + placebo: A 20 mg for 6 weeks - A 40 mg for 6 weeks - A 80 mg for 24 weeks. SUBJECTS: Forty-seven patients with hypercholesterolemia were recruited in four different outpatient clinics. MAIN OUTCOME MEASURES: Samples were obtained at randomization after 6, 12 and 36 weeks. Plasma or serum was analysed for lipids and for inflammation markers: C-reactive protein (CRP), serum amyloid A (SAA), soluble phospholipase A2 (SPLA2), intercellular adhesion molecule-1 (ICAM-1) and interleukin-6 (IL-6). RESULTS: The reduction in LDL was similar for the two statins, except at the highest dose of atorvastatin (41 vs. 47%). The increase in HDL tended to be more pronounced in the simvastatin group, significantly so on the highest dose of atorvastatin (P < 0.05). CRP and SAA was significantly reduced by atorvastatin, whilst no reduction was seen for simvastatin. There was a significant difference in treatment effects between the two statins. Both statins caused a reduction in SPLA2. For IL-6 and ICAM-1 only small and inconsistent reductions were observed for both statins. CONCLUSION: Atorvastatin reduced the liver-derived acute-phase reactants, CRP and SAA, whilst the effect of simvastatin was small or absent. Small and inconsistent effects were seen for both statins on plasma levels of IL-6 and ICAM-1.     

大黄对急性坏死性胰腺炎大鼠炎性介质表达的影响

目的 观察中药生大黄空肠灌注对急性坏死性胰腺炎(ANP)大鼠胰腺组织炎性介质表达的影响.方法 SD大鼠33只,按完全随机法分为对照组、ANP组及生大黄治疗组,每组11只.胰胆管逆行注射3％牛磺胆酸钠溶液方法制备ANP模型,同时做空肠造瘘.生大黄组于造模后空肠灌入1 g/ml生大黄煎液1ml/kg体重.造模36 h后处死大鼠.取血测定淀粉酶活性;取部分胰腺组织常规病理检查;取部分胰腺组织抽提总mRNA,采用实时PCR方法测定胰腺组织IL-6、IL-8、TNF-α mRNA表达.结果 造模后大鼠血淀粉酶活性明显升高,胰腺组织大片坏死、出血,大量炎细胞浸润,符合ANP改变.对照组胰腺组织IL-6、IL-8、TNF-αt mRNA表达量分别为0.29±0.13、0.35±0.15、1.09±0.32;ANP组分别为2.23 ±0.49、2.26±0.51、5.24±0.59,均较对照组显著增加(P值均＜0.05);生大黄组分别为0.97±0.30、1.02±0.34、2.59±0.36,均较ANP组显著减少,但仍显著高于对照组(P值均＜0.05).结论 生大黄空肠灌注治疗ANP大鼠可减少胰腺组织IL-6、IL-8、TNF-α mRNA的表达,从而减轻胰腺的病理损伤.     

Effect of metoprolol on myocardial apoptosis and caspase-9 activation after coronary microembolization in rats

OBJECTIVE:

To explore the effect of metoprolol on myocardial apoptosis and caspase-9 activation after coronary microembolization (CME) in rats.

METHODS:

Forty rats were randomly divided into four groups (n=10 each): a sham operation (control) group, CME plus saline (CME) group, CME plus metoprolol (metoprolol) group and caspase-9 inhibitor Z-LEHD-FMK (ZLF) group. CME was induced by injecting 3000 polyethylene microspheres (42 μm diameter) into the left ventricle during a 10 s occlusion of the ascending aorta. Echocardiography, terminal deoxynucleotidyl transferase dUTP nick end labelling and Western blotting were used to evaluate cardiac function, apoptosis and activation of caspase-9/caspase-3, respectively, 6 h after CME.

RESULTS:

The echocardiographic parameters of left ventricular function were significantly decreased in the CME group compared with the control group (P<0.05); however, the metoprolol group and ZLF group showed significantly improved cardiac function compared with CME alone (P<0.05). Compared with the control group, the myocardial apoptosis rate and the levels of activated caspase-9 and -3 increased significantly in the CME group (P<0.05). Again, these effects were ameliorated by metoprolol and ZLF (P<0.05).

CONCLUSIONS:

The present study demonstrates that metoprolol and ZLF can protect the rat myocardium during CME by inhibiting apoptosis and improving cardiac function, likely by inhibiting apoptosis/ mitochondrial apoptotic pathway. These results suggest that antiapoptotic therapies may be useful in treating CME.